It can be distinguished because of the flaccid bullae (blisters), epidermal acantholysis (acantholysis means loss of intercellular connections resulting in loss of cohesion between keratinocytes), and intraepidermal blistering.
Pemphigus vulgaris is due to formation of autoantibodies against desmosomal proteins.
Not an answer choice but the reason they said "intact basal layer of keratinocytes adherent to the basement membrane" is to distinguish it from Bullous pemphigoid, which is where sutoantibodies against HEMIdesmosomes cause the keratinocyte layer to peel away from the basement membrane. The blisters are often tense in bullous pemphigoid as well.
waitingonprometricIf it helps you, I always remember bullous pemphigoiD affects a Deeper layer of keratinocytes (autoAbs to hemidesmosomes), and pemphigus vulgariS affects a more Superficial layer of keratinocytes (autoAbs to desmosomes).+7
jdc_mdI also remember this by pemphigus vulgaris being the more serious condition (vulgar) and it presents with popped blisters/bleeding so it looks really vulgar on presentation (flaccid=popped/ deflated so more superficial = desmosomes.) Then bullous pemphigoid usually has blisters that havent popped yet so you know its a deepr blister (hemidesmosomes) +
submitted by โcassdawg(1780)
This is Pemphigus Vulgaris (FA2020p480)
It can be distinguished because of the flaccid bullae (blisters), epidermal acantholysis (acantholysis means loss of intercellular connections resulting in loss of cohesion between keratinocytes), and intraepidermal blistering.
Pemphigus vulgaris is due to formation of autoantibodies against desmosomal proteins.
Not an answer choice but the reason they said "intact basal layer of keratinocytes adherent to the basement membrane" is to distinguish it from Bullous pemphigoid, which is where sutoantibodies against HEMIdesmosomes cause the keratinocyte layer to peel away from the basement membrane. The blisters are often tense in bullous pemphigoid as well.